New insights into the mechanism of fibroblast to myofibroblast transformation and associated pathologies

Mitchell Aaron Watsky, Karl T. Weber, Yao Sun, Arnold Postlethwaite

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

Myofibroblasts are a differentiated cell type essential for wound healing, participating in tissue remodeling following insult. Myofibroblasts are typically activated fibroblasts, although they can also be derived from other cell types, including epithelial cells, endothelial cells, and mononuclear cells. In most organ systems, cell signals initiated following tissue-specific insult or during the metastatic process lead to differentiation of fibroblasts or other precursor cells to the myofibroblast phenotype. In addition to their beneficial and necessary role in wound healing, myofibroblasts also contribute to a number of pathologies, primarily fibrotic processes and tumor invasiveness. This review explores both traditional and nontraditional concepts of myofibroblast differentiation in the cornea, skin, heart, and other tissues, as well as some of the pathologies associated with myofibroblast activities.

Original languageEnglish (US)
Pages (from-to)165-192
Number of pages28
JournalInternational Review of Cell and Molecular Biology
Volume282
Issue numberC
DOIs
StatePublished - Jan 1 2010
Externally publishedYes

Fingerprint

Myofibroblasts
Pathology
Fibroblasts
Tissue
Endothelial cells
Wound Healing
Tumors
Skin
Cornea
Endothelial Cells
Epithelial Cells
Phenotype
Neoplasms

Keywords

  • Cornea
  • Fibrocyte
  • Fibrosis
  • Heart
  • Lung
  • Scleroderma
  • Systemic sclerosis

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

New insights into the mechanism of fibroblast to myofibroblast transformation and associated pathologies. / Watsky, Mitchell Aaron; Weber, Karl T.; Sun, Yao; Postlethwaite, Arnold.

In: International Review of Cell and Molecular Biology, Vol. 282, No. C, 01.01.2010, p. 165-192.

Research output: Contribution to journalArticle

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